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find thickish, flat bundles of muscle which run through the middle of the ligaments, and during menstrual excitement enable contractions to take place, similar to those which we can follow with such great distinctness in external portions of the genital passages.

If now the question be raised how far the individual elements of the vessels are of importance in the body, it is at once evident that the contractile elements play the most important part in the coarser processes of the circulation, whilst the elastic constituents come next, and the simply permeable, homogeneous membranes last. Let us first consider the import of the muscular elements, and more particularly in those vessels which are chiefly provided with them, namely the arteries.

When an artery is acted upon by any influence which causes a contraction of its muscular tissue, it must of course become narrower, inasmuch as the contractile cells lie in rings around the vessel; this contraction may under certain circumstances proceed until the canal is almost entirely obliterated, and the natural consequence then is that less blood penetrates into the corresponding part of the body. When therefore an artery is in any way exposed to a pathological irritant, or when it is excited by some physiological stimulus, its proper action cannot be displayed in any other way than by its becoming narrower. Now, indeed, that the muscular elements of the walls of the vessels have become known, the old doctrine might again be taken up, that, namely, the vessels, like the heart, originated a kind of rhythmical pulsating movement, which was capable of directly furthering the onward movement of the blood, so that an arterial hyperemia would be the result of an increased pulsation in the vessels.

We are indeed acquainted with one isolated fact which is a proof that a real rhythmical movement does take place in

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the arterial walls; and this was first observed by Schiff in the ears of rabbits. Its rhythm, however, does not at all correspond with that of the well-known arterial pulsation; the only counterpart to it exists in the movements which had previously been observed by Wharton Jones in the veins of the wings of bats, and proceed in an extremely slow and quiet manner. I have studied these phenomena in bats, and convinced myself that the rhythm coincides neither with the cardiac nor the respiratory movements; it is quite a peculiar, but comparatively not very forcible, movement, and takes place after tolerably long pauses, longer ones than are observed in the case of the circulation and shorter than those which occur in respiration. In the ears of rabbits also the contractions of the arteries are far slower than the cardiac and respiratory movements.

After excluding these phenomena, which manifestly ought not to be explained in such a way as to support the old view of the local occurrence of pulsation, the essential fact remains, that the muscular fibres of a vessel contract upon the application of every stimulus which sets them in action, but that this contraction is not propagated in a peristaltic manner, but is confined to the spot irritated, or at most extends a little beyond, and continues for a certain length of time at this spot. The more muscular the vessel is, the more lasting and forcible is the contraction and the greater is the obstruction experienced by the current of blood. The smaller the vessels, the more rapidly, on the contrary, do we see the contraction succeeded by a dilatation, which, however, is not in its turn followed by a contraction, as it would have to be to constitute a pulsation, but persists for a longer or shorter time. This dilatation is not of an active, but of a passive, nature, and results from the pressure of the blood upon the wall of the vessel which has become fatigued and opposes less resistance.

If we now proceed to examine the phenomena which are usually grouped together under the title of active hyperæmia, there can be no doubt but that the muscular tissue of the arteries is generally essentially concerned therein. We very commonly find we have to deal with processes in which the muscular fibres of the vessels have really been stimulated, and the contraction is succeeded by a state of relaxation,

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Fig. 49. Irregular contraction of small vessels from the web of a frog's foot after the application of stimuli. Copied from Wharton Jones.

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such as scarcely ever occurs in an equally marked manner in the rest of the muscles, a state which is manifestly the expression of a kind of fatigue and exhaustion, and is the longer persistent, the more energetic the stimulus which was applied. In small vessels with few muscular fibres, therefore, it often seems as if the stimuli really induced no contraction, in consequence of the extreme rapidity with which a state of relaxation is seen to set in, continuing for a considerable time, and allowing of an increased influx of blood.

This same condition of relaxation we can experimentally most easily produce by cutting the nerves supplying the vessels of a part, whilst the contraction can be effected to a very great extent by submitting these nerves to a very energetic stimulus. That our acquaintance with this kind of contraction is of so late a date, is explained by the fact that the stimuli applied to the nerves must be very powerful, and that, as Claude Bernard has shown, only strong electrical currents are sufficient for the purpose. On the other hand, the conditions which ensue upon the section of the nerves are in most parts so complicated, that the dilatation escaped observation, until the lucky spot was discovered also by Bernard, and by the section of the sympathetic nerves in the neck a reliable and convenient field for observation was thrown open to experiment.

We obtain therefore the important fact that, whether the widening of the vessel, or, in other words, the relaxation of its muscular fibres, be produced directly by a paralysis of the nerve or an interruption of the nervous influence, or whether it be the indirect result of a previous stimulation, giving rise to exhaustion-that, I say, in every case we have to deal with a kind of paralysis of the walls of the vessel, and that the process is incorrectly designated active hyperæmia, inasmuch as the condition of the vessels in it is always a completely passive one. All that has been built up upon

this assumed activity of the vessels, is, if not exactly built upon sand, still of an extremely ambiguous nature, and all the conclusions that have besides been drawn with regard to the important influence which the activity of the vessels was supposed to have upon the conditions of nutrition of the parts themselves, fall at the same time to the ground.

When an artery is really in action, it gives rise to no hyperæmia; the more powerfully it acts, the more does it occasion anæmia, or, as I have designated it, ischemia, and the less or greater degree of activity in the artery determines the greater or less quantity of blood which in a unit of time can stream into a given part. The more active the vessel, the less the supply of blood. If then we have to deal with an hyperæmia the result of irritation, the most important point, therapeutically, is just this, to place the vessels in such a state of activity as will enable them to offer resistance to the onward rush of blood. This we can accomplish by the means of what is called counter-irritation, a higher degree of irritation in an already irritated part, stimulating the fatigued muscular fibres of the vessel to persistent contraction, and thereby diminishing the supply of blood and leading the way to a regulation of the disturbance. In the very cases in which reaction, that is, regulatory activity, is most called for, the chief point is to overcome that state of passiveness which maintains the (so-called active) hyperæmia.

If we now pass from the muscular to the elastic constituents of the vessels, we meet with a property which is of very great importance, on the one hand in the veins, the activity of which is in many cases to be wholly referred to their elastic elements, on the other hand in the arteries and particularly in the aorta and its larger branches. In these the elasticity of the walls has the effect of compensating for the loss which the pressure of the blood experiences from the systolic dila

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